Background and objectives: Thalassemia patients have alterations in the exp
ression of some activation and adhesion molecules on peripheral blood lymph
ocytes. We studied cell surface antigens on peripheral blood cells associat
ed with the activation of these cells and soluble molecules produced by act
ivated endothelium. Design and methods: We investigated the expression of C
D11b, CD18, CD35, CD43, CD44, and CD69 on the peripheral blood monocytes, C
d11b, CD18, CD35, CD43, CD44, CD67 on peripheral blood neutrophils and CD38
and CD69 on peripheral blood lymphocytes. We studied 68 transfusion-depend
ent thalassemics (group A), 10 transfusion non-dependent thalassemics (grou
p B), 18 beta -thalassemia carriers (group C), and 28 normal individuals. R
elative fluorescence intensity was used to determine the antigen density. A
nalysis was performed with an EPICS ELITE flow cytometer. Furthermore, solu
ble intercelullar adhesion molecule 1 (sICAM-1), soluble vascular adhesion
molecule 1 (sVCAM-1), and E-selectin, tumor necrosis factor (TNF) alpha, an
d interleukin (IL) 1 beta were measured in the plasma of patients by enzyme
-linked immunometric assay. Results: The expression of CD11b, CD18, and CD6
9 on the monocytes of group A was significantly greater than in groups B an
d C and in controls, while CD44 was significantly downregulated in group A.
CD11b, CD 18, CD35, CD44, and CD67 on the surface of neutrophils and CD38
and CD69 on the surface of lymphocytes were also overexpressed in group A.
CD44 was downregulated on the monocytes and upregulated on the neutrophils
of the patients compared to controls. The levels of sICAM-1, sVCAM-1, E-sel
ectin, TNF-alpha, and IL-1 beta in the serum of patients in groups A and B
were higher than those in group C and the controls. Conclusion: Endothelial
activation markers are significantly increased in thalassemia patients, an
d activated blood cells circulate in the peripheral blood. These may be rel
ated to the vascular complications in these patients and might be useful ma
rkers for the follow-up of the vascular disease.